Paediatric pneumonia? Lung Ultrasound.

If you are a regular reader then you will know that I have been spruiking lung ultrasound for a few years now.  In fact I wrote this post [ Ultrasound for pneumonia – sounds crazy? ]  way back in early 2012.  There continues to be a slow trickle of studies looking at US for pneumonia – and like a lot of US literature – the numbers are small in each paper.

In March 2015 Pediatrics published a systematic review titled:

Lung Ultrasound for the Diagnosis of Pneumonia in Children: A Meta-analysis by Perada et al.  This was a metanalysis of 8 smaller studies (2 in neonates) which showed that lung US performed well as a diagnostic tool compared to CXR.  The papers used a variety of “US users” from expert to novice sonographers.

The diagnostic characteristics have been reasonably variable across these small trials and they give the following as their overall analysis of lung US for pneumonia:

  • Sensitivity 96%,  Specificity  93%,
  • + Likelihood ratio = 15.3      -ve Likelihood ratio = 0.06
  • if you are into “area under the ROC” – it was 0.98 – which is pretty good!

These figures are our best estimate of the utility of LUS for pneumonia in kids.  They are significantly better than the characterisitics of traditional plain film.

So, are we there yet?  Is there enough evidence to change practice?

I think that there is.

Lung US is at least “non-inferior” to CXR.  US carries no risk of radiation and is a fast and technically easy scan to do in small people.  The cost is …  a few dollops of gel and the time to do the scan.

There will certainly be a risk of overdiagnosis given the relatively high sensitivity of US and the potential to misinterpret findings.  This is going to require education and training around image interpretation.  As with all point-of-care US – one needs to interpret the images in the clinical context and be prepared to do another test if the data doesn’t make sense.

So I would love to hear your thoughts –

  • is there enough here to change practice?
  • what barriers are there in your practice to change imaging preferences?

Let me know.



Extreme Bradycardia after Diarrhea and Dehydration. Best ED treatment?

A patient presented with weakness.  He was found to be bradycardic, so this ECG was recorded:
There is atrial flutter with 3rd degree AV block and Left ventricular escape.  Why is it not slow AV conduction with RBBB?  The QRS occurs at different points on the flutter wave.  There is complete dissociation due to complete AV block.

More history

The patient has a history of congenital heart disease repaired as a child. He reports having had an extra pacemaker transiently but this was removed at a very young age. The patient describes a history of progressive bradycardia. In recent years, the patient states that his heart rate has generally been in the 30s. 

The patient states that he developed a gastrointestinal illness in recent days. This was associated with nausea and recurrent episodes of vomiting. He had decreased oral intake. The patient describes having taken potassium supplementation in recent days. Today, the patient became increasingly lightheaded. He took his pulse and felt that it was in the teens. He presented to the emergency department for further evaluation.

In the emergency department, the patient's heart rate was between 10 and 15.  EKG revealed atrial flutter with junctional rhythm. Laboratory studies revealed an elevated creatinine at 2.9 mg/dL and a K of 5.4 mEq/L. 

What is the best first ED treatment?  See below.

The patient has had bradycardia for years, but never this bad.  He clearly has chronic AV block, but why did it get so bad right at this moment?

Because his gastrointestinal illness led to renal insufficiency, which with K supplementation led to mild hyperkalemia of only 5.4 mEq/L, which was just high enough to tip him over the edge.

The best fast treatment is to treat hyperK with Calcium, insulin and glucose, and possibly bicarbonate.  One may add beta-2 agonists:

Terbutaline and Albuterol for Lowering of Plasma Postassium

The patient clearly needs a permanent pacemaker, but only needs an emergent ED pacemaker if treatment of hyperK does not work.

Emergency Transvenous Cardiac Pacing

A Call to Retire Routine C-Spine Immobilization

Remember the heartwarming children’s tale of the young woman with the ribbon around her neck?  Once removed, the head falls from the body, and the unfortunate woman expires.  Thus, the inspiration and evidential basis for modern trauma care utilizing immobilization of the cervical spine.

This article asks a very simple question: is there evidence to support the notion of incidental cerebrospinal movement resulting in subsequent paralysis?  Their answer: probably not.

These authors review several thousand abstracts to extract twelve publications describing a mere 41 cases of patients who were not completely immobilized, and thence suffered subsequent neurologic deterioration.  The individual cases reported upon provide, generally, rather spotty detail regarding the circumstances.  Some patients had additional falls or trauma in the ED, others were intoxicated and combative, while many others seemed to have gradual worsening without a specific event.

These authors propose this gradual worsening represents the primary time scale of neurologic deterioration – and suggest the suspected precipitating events documented by these cases represent contextual red herrings.  Rather than becoming tetraplegic as a consequence of repositioning in the Emergency Department, it is more likely clinical manifestations result from ligamentous disruption, bleeding, and edema related to the primary injury, and immobilization would not have prevented their progression.

Of course, this paucity of documented examples cannot represent an exhaustive report of all known secondary deterioration after an initial, non-immobilized injury.  However, just as erroneous is the presumption that immobilization prevents such secondary deterioration – particularly when coupled with the known inconveniences and harms of mass immobilization during transport and evaluation.

It’s time for routine cervical spine immobilization to go!  However, such discontinuation need be undertaken in such a setting as capable of detecting any adverse events resulting from such.

“Early Secondary Neurologic Deterioration After Blunt Spinal Trauma: A Review of the Literature”

Hypertensive Crisis in Kids

Originally published at Pediatric EM Morsels on May 17, 2013. Reposted with permission.

Follow Dr. Sean M. Fox on twitter @PedEMMorsels


I think that we’d all agree that 144/89 is not a normal blood pressure, but it is one that those of us who have the pleasure of caring for adults will look at with almost a sense of comfort – because it isn’t 70/30 or 210/120.  Unfortunately, however, this sense of reassurance cannot be had when dealing with children. Depending on the patient’s sex, age, and height, 144/89 may not only represent hypertension but may be associated with hypertensive crisis in kids!

Hypertension in Kids

  • Kids are becoming more and more like “little adults.”
    • The prevalence of hypertension in kids is increasing.
      • Likely associated with increases in obesity and metabolic syndrome.
    • Kids also now with increasing prevalence of biliary disease and kidney stones.
  • Naturally, normal blood pressure varies with the age of the patient.
    • For low blood pressures, we’ve discussed using the formula goal SBP = 90 + (2 x Age).
    • Normal blood pressure is defined as SBP and DBP < the 90th percentile for sex, age, and height.
    • Hypertension is defined as SBP and DBP > 95th percentile for sex, age, and height.
    • THERE ARE CHARTS!  Use them to determine the percentile… you can’t remember these numbers (or at least I cannot).
  • Hypertension in kids is more likely to be secondary to another concerning cause.
    • Adolescents have a higher incidence of essential hypertension, but should still have secondary causes investigated (see case of Coarctation).
    • Some important etiologies to consider:
      • Renal Pathology
        • Glomerulonephritis
        • Hemolytic Uremic Syndrome
        • Wilm’s Tumor
        • Nephrotic syndromes
        • Polycystic kidney disease
        • Renovascular disease
      • Coarctation of the Aorta
      • Neuroendocrine
        • Neuroblastoma
        • Pheochromocytoma
        • Thyroid disease
      • Collagen Vascular Disease
        • Lupus
        • Periarteritis nodosa
      • DRUGS (especially with those crafty teenagers)
        • Decongestants
        • Anabolic Steroids
        • Cocaine

Hypertensive Crisis in Kids

  • Hypertensive crisis occurs when there is accelerated hypertension in association with end-organ damage.
  • Common symptoms:
    • Headache (#1 complaint)
    • Nausea & Vomiting
    • Chest Pain / Left heart failure
    • Dizziness
    • Convulsions
    • Status Epilepticus
    • Coma
  • Initial Evaluation
    • Four Limb pulses and blood pressures
    • CXR
    • Chemistry panel
    • Urinalysis
    • Fundoscopic exam (papilledema?)
    • Abdominal bruits?
    • Draw and hold additional blood for subspecialist’s requests (ex, renin and aldoesterone levels)
  • Some Therapeutic Options
    1. Nicardipine: FIRST LINE Tx. no negative inotropic effects. – onset ~15 min, 1/2 life = 10-15 min
    2. Labetalol: potentially worsens hyperkalemia. Has negative inotropic effects. 1/2 life 3-5 hrs.
    3. Nitroprusside: Need to keep cyanide toxicity on your radar screen!
    4. Esmolol: Useful after congenital heart disease repair. 1/2 life 10 min.
    5. Fenoldopam: Safe with renal disease. Increases renal blood flow and induces natriuresis.
  • GOAL: Decrease blood pressure by no more than 25-30% of original value during first 8 hrs.

Convulsion due to HTN or HTN due to Convulsion?

  • Hypertensive crisis can provoke convulsions: Seizures can increase blood pressure.
  • How can you differentiate between the two and select the most appropriate therapies?
  • Study published in Critical Care Medicine found that a SBP or DBP of greater than 4 Standard Deviations above the average for the age is 78% predictive for the presence of hypertensive crisis. Values lower than this level had a negative predictive value of 100% (excluded hypertensive crisis).
  • The Cutoff BP = ([4 x Standard Deviation for age] + Mean BP for age); which equates to the following:
    • Girls:
      • 1 mnth – 130/97
      • 1 yr – 144/89
      • 6 yrs – 137/100
      • 12 yrs – 153/106
    • Boys
      • 1 mnth – 126/95
      • 1 yr – 143/89
      • 6 yrs – 136/98
      • 12 yrs – 149/105

 Proulx F, LaCroix J, Farrell CA, Gauthier M. Convulsions and hypertension in children: differentiating cause from effect. Critical Care Medicine. 1993; 23: 1541-1546.

Chadar J, Zilleruelo G. Hypertensive crisis in children. Pediatric Nephrology. 2012; 27: 741-751.

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